Pulmonary fibrosis is characterized by hyperplasia of stromal cells due to formation of bundles of collagen and the like produced by proliferative fibroblasts in alveolar walls, and is a disease whose cardinal symptoms are dry cough and exertional dyspnea. This disease is caused by progression from interstitial pneumonia, and in many cases, interstitial pneumonia can be the preliminary symptom. Prognosis of interstitial pneumonia is poor and, in many cases, interstitial pneumonia progresses to pulmonary fibrosis. There are many cases where the interstitial pneumonia, in which the cause can be identified, is cured by removing the cause or by administering anti-inflammatory agents such as steroids; however, for the case of unexplained idiopathic interstitial pneumonia, no radical treatments currently exist, and treatments, such as administration of steroids, azathioprine, cyclophosphamide and the like when the symptoms worsen, and oxygen therapy when hypoxemia is caused, are performed at the best. If unexplained idiopathic interstitial pneumonia progresses to pulmonary fibrosis, about the half of the pulmonary fibrosis patients die within 5 years from occurrence of the symptoms. Because of this, interstitial pneumonia is designated as one of the specified intractable diseases in Japan.
On the other hand, it has been known that prostaglandin E2 (hereinafter, abbreviated as “PGE2”) has a wide variety of bioactivities as a metabolic product in the arachidonic acid cascade, and acts as an agonist against four receptors that are EP1, EP2, EP3, and EP4. Recently, it has been reported that the EP2 receptor is a receptor that is related to inhibition of pulmonary fibroblast proliferation and collagen formation via PGE2 (see Non-Patent Document 1). Furthermore, it has been suggested that the EP2 receptor is also a receptor that is related to inhibition of apoptosis of alveolar epithelial cells via PGE2 (see Non-Patent Document 2). Therefore, a compound that exhibits agonistic effect like that of PGE2, and in particular, a compound that exhibits effect of EP2 selective agonist is expected to be a therapeutic agent and/or prophylactic agent for interstitial pneumonia and pulmonary fibrosis.
So far, it has been disclosed that a prostanoid-based compound exhibiting EP2 agonistic effect is useful for prophylaxis and/or therapy of respiratory diseases including pulmonary fibrosis (see Patent Documents 1 and 2). Furthermore, a non-prostanoid-based compound exhibiting EP2 agonistic effect has been also known (see Patent Documents 3 to 17). Among these, various diseases that are exemplified as the targets of the medical use of the compounds described in Patent Documents 9 and 11 to 17 include pulmonary fibrosis. However, in Patent Documents 9 and 11 to 17, there are no specific descriptions regarding pharmacological test examples in which these compounds are useful for pulmonary fibrosis. Furthermore, there are no specific descriptions in any of these Patent Documents regarding working examples of a sulfonamide compound related to the present invention having, as its partial structure, a biaryl group in which a particular substituent is substituted at a particular part.